STAT1/3-IN-1
Based on 3 publication(s) in Google Scholar
STAT1/3-IN-1 is a potent STAT1/3 inhibitor with potent anti-inflammatory effect. STAT1/3-IN-1 inhibits phosphorylation and nuclear translocation of STAT1/3 to modulate microglial inflammation, reduces LPS (HY-D1056)-induced pro-inflammatory cytokines (NO, IL-1β, IL-6, and TNF-α) and inflammatory mediators (iNOS, COX-2). STAT1/3-IN-1 exhibits low toxicity in mice. STAT1/3-IN-1 can be used for the research of neuroinflammation.
For research use only. We do not sell to patients.
- Purity : 99.23%
- CAS No.: 2958649-56-2
- Formula: C28H25ClN6O5
- Molecular Weight:560.99
-
Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
-
Solvent & Solubility
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Publications Citing Use of MedChemExpress (MCE) STAT1/3-IN-1
More
Biological Activity
Description
IC50 & Target
[1]|
COX-2 |
IL-6 |
iNOS |
STAT3 |
STAT1 |
IL-1β |
TNF-α |
In Vitro
STAT1/3-IN-1 (compound 6k) (1-10 μM, 26 h) inhibits LPS-induced NO production with an IC50 of 4.45 μM, while maintains cell viability in BV-2 cells[1].
STAT1/3-IN-1 (5-10 μM; 8 h) significantly downregulates mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and inflammatory mediators (iNOS, COX-2) in LPS-stimulated BV-2 cells[1].
STAT1/3-IN-1 (5-10 μM) reduces LPS-induced IL-6 and TNF-α release in BV-2 cells[1].
STAT1/3-IN-1 (5-10 μM; 26 h) dose-dependently reduces iNOS and COX-2 protein expression in LPS-stimulated BV-2 cells[1].
STAT1/3-IN-1 (5-10 μM; 5 h) inhibits STAT1 and STAT3 phosphorylation and reduces nuclear phosphorylated STAT1 and STAT3 in LPS-stimulated BV-2 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:5, 10 μM
-
Incubation Time:8 h (2 h pretreatment + 6 h with LPS)
-
Result:Significantly downregulated mRNA expression of IL-1β, IL-6, TNF-α, iNOS and COX-2 in LPS-stimulated BV-2 cells.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:5, 10 μM
-
Incubation Time:26 h (2 h pretreatment + 24 h with LPS)
-
Result:Decreased LPS-induced iNOS and COX-2 protein expression in a concentration-dependent manner.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:5, 10 μM
-
Incubation Time:5 h (2 h pretreatment + 3 h with LPS)
-
Result:Abrogated LPS-induced phosphorylation of STAT1 and STAT3.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:10 μM
-
Incubation Time:5 h (2 h pretreatment + 3 h with LPS)
-
Result:Significantly reduced nuclear presence of phosphorylated STAT1 and STAT3 under LPS stimulation.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:10 μM
-
Incubation Time:5 h (2 h pretreatment + 3 h with LPS)
-
Result:Decreased levels of phosphorylated STAT1 and STAT3 in nuclear extracts under LPS stimulation.
-
Cell Line:LPS-stimulated BV-2 cells
-
Concentration:1, 10 μM
-
Incubation Time:26 h (2 h pretreatment + 24 h with LPS)
-
Result:Showed no significant cytotoxicity, with cell viability of 88.03% (1 μM) and 86.71% (10 μM) compared to the control group.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
-
Animal Model:Male and female KM mice[1]
-
Dosage:250 mg/kg
-
Administration:i.g.; single dose
-
Result:Showed no significant differences in body weight, organ indices, GPT and GOT levels compared to vehicle control.
Showed no significant damage in major organs (heart, liver, spleen, lungs, and kidneys).
Chemical Information
-
CAS No. 2958649-56-2
-
Appearance Solid
-
Molecular Weight 560.99
-
Formula C28H25ClN6O5
-
Color White to off-white
-
SMILES
ClC1=C(N2C=C(C3=CC=CC(NC(C4=CN(C[C@@](OCC[C@H]5C)([H])N5C6=O)C6=C(OC)C4=O)=O)=C3)N=N2)C=CC=C1
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (3)
-
Journal Impact Factor
-
Most Recent
-
-
Phytother Res
(+)-Matairesinol, Derived From Olive Oil, Enhanced T-Cell Anti-Tumor Immune via JAK3-STAT1 Signal and Synergized With Anti-PD-1 Efficacy. [Abstract]2026 Apr 27. PMID: 42037203 -
J Ethnopharmacol
"Shihu" promote T-cell immunity against breast cancer through bioactive constituent THMB enhancing JAK3-STAT1 signal. [Abstract]2026 Oct 28:369:121888. PMID: 42202911
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (178.26 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
-
-
-
-
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
-
%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
-
%+
-
+%Tween-80 + +
-
%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocols
-
Kinase activity and phosphorylation assays
Kinase activity assays measure the ability of kinases to transfer phosphate groups from ATP to specific substrates, while phosphorylation assays detect the presence and levels of phosphorylated proteins. Common methods include radiolabeled ATP incorporation (e. g. ,), ADP release detection via bioluminescence (e. g. ,[3]), enzyme-linked immunosorbent assays (ELISA) for phospho-specific epitopes (e. g. ,[6]), and microtiter-based formats for high-throughput screening (e. g. ,[8]). The ADP-Glo assay quantifies kinase activity by measuring ADP produced during phosphorylation using a luciferase-based system. Radiometric assays involve autoradiography or scintillation counting after incorporation of 32P-labeled ATP into substrate proteins. ELISA-based approaches rely on phospho-specific antibodies to detect activated kinases in cell lysates or purified samples.
-
Western Blot
Western blotting (WB) is a commonly used experimental method in molecular biology, biochemistry, and immunogenetics for identifying and quantifying target proteins. It combines gel electrophoresis with immunoassay, enabling researchers to analyze protein expression, post-translational modifications, and molecular weight.
-
Cytoplasmic-Nuclear Fractionated Protein Extraction
Cytoplasmic-nuclear fractionated protein extraction separates soluble cytoplasmic proteins from nuclear-enriched proteins by mild plasma-membrane permeabilization, differential centrifugation, washing of nuclei, and extraction of nuclear proteins for downstream immunoblotting or related molecular analysis. The readout is the relative abundance of a protein in cytoplasmic and nuclear fractions, commonly assessed by western blotting together with compartment markers such as tubulin or pyruvate kinase for cytoplasm and lamin, nucleoporin, hnRNP, H2AX, or Lamin B for nuclear fractions.
-
LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
-
Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
-
Protocol for Kinase activity and phosphorylation assays
Kinase activity assays measure transfer of phosphate from ATP to a protein or peptide substrate, generating phosphorylated substrate, ADP, or incorporated radiolabeled phosphate as the readout; phosphorylation assays measure site-specific phosphorylation in cells or tissues as a proxy for kinase-pathway activation, inhibition, or substrate regulation. Phosphorylation can be detected by phospho-specific Western blot, immunoprecipitation kinase assay, phospho-immunofluorescence, phospho-flow cytometry, luminescent ADP detection, radiolabeled ATP incorporation, or reporter-based pathway assays, and these readouts can be applied to cancer cells, primary neurons, mouse tumors, organoids, inflammatory macrophages, ferroptosis studies, and mitophagy studies when the kinase target is biologically relevant.
-
Research Protocol for Neurological Diseases
PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie
-
Pyroptosis Solutions
Pyroptosis is a lytic inflammatory cell-death pathway executed by gasdermin pores, most classically through inflammasome-mediated activation of caspase-1, cleavage of gasdermin D, membrane pore formation, LDH release, and secretion of IL-1β and IL-18. The canonical pathway is commonly modeled by priming cells with an inflammatory signal such as LPS to induce pro-IL-1β and inflammasome components, followed by an activation signal such as ATP or nigericin to activate NLRP3, ASC speck formation, caspase-1 cleavage, GSDMD cleavage, cytokine release, and pyroptotic membrane rupture. The non-canonical pathway is triggered when cytosolic LPS activates mouse caspase-11 or human caspase-4/5, leading to GSDMD cleavage and pyroptosis, and this can secondarily activate NLRP3-dependent IL-1β release. Pyroptosis is linked to inflammatory injury, infection, cancer, liver disease, ocular disease, placental inflammation, and other disease phenotypes, but unresolved questions include which gasdermin fam
Purity & Documentation
-
Data Sheet (280 KB)
-
SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
-
Handling Instructions (2659 KB)
References
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 1.7826 mL | 8.9128 mL | 17.8256 mL | 44.5641 mL |
| 5 mM | 0.3565 mL | 1.7826 mL | 3.5651 mL | 8.9128 mL | |
| 10 mM | 0.1783 mL | 0.8913 mL | 1.7826 mL | 4.4564 mL | |
| 15 mM | 0.1188 mL | 0.5942 mL | 1.1884 mL | 2.9709 mL | |
| 20 mM | 0.0891 mL | 0.4456 mL | 0.8913 mL | 2.2282 mL | |
| 25 mM | 0.0713 mL | 0.3565 mL | 0.7130 mL | 1.7826 mL | |
| 30 mM | 0.0594 mL | 0.2971 mL | 0.5942 mL | 1.4855 mL | |
| 40 mM | 0.0446 mL | 0.2228 mL | 0.4456 mL | 1.1141 mL | |
| 50 mM | 0.0357 mL | 0.1783 mL | 0.3565 mL | 0.8913 mL | |
| 60 mM | 0.0297 mL | 0.1485 mL | 0.2971 mL | 0.7427 mL | |
| 80 mM | 0.0223 mL | 0.1114 mL | 0.2228 mL | 0.5571 mL | |
| 100 mM | 0.0178 mL | 0.0891 mL | 0.1783 mL | 0.4456 mL |
STAT1/3-IN-1 Related Classifications
HY-170621 Related Classifications
Powered by Bioz